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Jerky Pet Treats Update

Jerky Pet Treats Update

The FDA has recently released an official product safety report on chicken jerky pet treats.  Warnings have been issued since 2007 against the use of these products due to their apparent correlation with renal failure, yet as of September 2013 over 3000 complaints have been filed.

FDA Report

Notable links included in the report consist of a Fact Sheet for Pet Owners (vets are encouraged to distribute this to their clients).

An analytical results summary of this investigation performed by the FDA and various VET-LIRN laboratories is published in the Investigation Rationale and Results.

WVDL is a Vet-LIRN lab.

During 2007, FDA noted a number of adverse event consumer complaints associated with consumption of jerky pet treats. Product testing did not identify a causative agent, thus FDA issued a cautionary warning regarding chicken jerky products to consumers in 2007 and a Preliminary Animal Health Notification in 2008. There were fewer complaints during 2009 and 2010, but increasing numbers in 2011 generated a third FDA warning in November of the same year. As of September 24, 2013, FDA has received approximately 3000 reports of pet illnesses which may be related to consumption of the jerky treats.

Vet-LIRN became actively involved in pet jerky treats investigation at the end of 2011. We obtain medical histories of pets that have been seen by a veterinarian, and based on the case profile, we plan and organize testing of treats collected from the consumer. Testing is performed by FDA laboratories and other animal health diagnostic laboratories in our network. Vet-LIRN also coordinates collection and testing of diagnostic material and tissues from affected animals. Our cooperation with experts from government and veterinary diagnostic laboratories across the country will provide a high level of professional expertise to provide greater insight into pet jerky treats related illness. The most recent document describing the Investigation Rationale and Results was posted October 22, 2013.


PCR Assays developed at WVDL help identify cause of death of Bison

PCR Assays developed at WVDL help identify cause of death of bison


Dr. Scott Jones Diagnostic Pathologist and Supervisor, Barron Lab DVM, Michigan State Univ., 1978

Dr. Scott Jones
Diagnostic Pathologist and Supervisor, Barron Lab
DVM, Michigan State Univ., 1978



The cause of death of a bison at the Irvine Park Zoo in Chippewa Falls was recently solved by Dr. Jones by using one of the diagnostic PCR assays developed at WVDL.  Blood from the  bison tested positive for  malignant catarrhal fever (MCF) an uncommon but deadly disease in bison. Read more about the incident here:


Epizootic Hemorrhagic Disease (EHD) confirmed in Wisconsin cattle

Epizootic Hemorrhagic Disease (EHD) confirmed in Wisconsin cattle

MADISON –Animal health officials are urging cattle farmers to take preventive measures against Epizootic Hemorrhagic Disease (EHD) in cattle in light of two recent confirmed illnesses.   The Wisconsin State Veterinarian encourages the use of insect control to eliminate biting midges and black flies, which are common carriers of the disease that primarily affects deer, but can also infect cattle and other ruminants.

“We already have reports of EHD in Wisconsin cattle, and until we have a hard freeze to kill the midges and flies, the virus will continue to be a threat to our cattle population,” said Dr. Paul McGraw, State Veterinarian.

EHD in cattle is rare, but can happen when environmental conditions support insect growth.  Signs include fever, ulcers in the mouth and gums, swollen tongue, excessive salivation, and lameness or stiffness when walking. Death loss is uncommon in cattle.  There is no evidence that the EHD virus can infect humans or that it is transmitted between animals.

“The symptoms of EHD are similar to those of Foot and Mouth Disease.  So, farmers who notice signs of illness in cattle are encouraged to immediately contact their veterinarian to rule out a possible foreign animal disease,” McGraw said.


Dr. Donald Sockett Findings From Bovine Respiratory Disease (BRD) Study

 Dr. Donald Sockett Presents Poster on BRD


On Friday, Sept. 20, Dr.  Donald Sockett gave a poster presentation on bovine respiratory disease (BRD) at the American Association of Bovine Practitioners (AABP) Annual Conference in Milwaukee.  The most interesting findings of this study follow.  The link to view Sockett’s poster is included below.

Dr. Donald Sockett Veterinary Microbiologist DVM, Univ. of Guelph, 1981 PhD, Univ. of Wisconsin, 1991 Diplomate, A.C.V.I.M.

Dr. Donald Sockett
Veterinary Microbiologist
DVM, Univ. of Guelph, 1981
PhD, Univ. of Wisconsin, 1991
Diplomate, A.C.V.I.M.

  • Mycoplasma bovis and bovine respiratory corona virus were found in a high number of calves (≥ 50%) with BRD.
  • Treated calves with BRD consumed less dry feed (calf starter) and had poorer feed-to-gain ratios than calves that did not have BRD.
  • There was no difference in milk replacer consumption between calves with BRD (even if treated) and calves that did not have BRD, thus indicating that a reduction in liquid feed ( milk or milk replacer) intake is not a reliable metric to use for early detection of BRD.
  • Even if treated, calves with BRD weighed less at weaning time than calves that did not have BRD.
  • Pre-weaned calves that had a bout of BRD severe enough to require treatment with antimicrobial drugs should be fed milk or milk replacer for a longer period of time than calves that have not had BRD. The longer feeding time will give the BRD affected calves the time they need to catch up (growth) with the calves that did not have BRD.


Poster for Presentation

Elevated Copper Levels Affecting Wisconsin Holsteins

Copper Accumulation in Wisconsin Holsteins



Dr. Doug Lyman Diagnostic Pathologist DVM, Iowa State 1981 Diplomate, A.C.V.P

Dr. Doug Lyman
Diagnostic Pathologist
DVM, Iowa State 1981
Diplomate, A.C.V.P

By Dr. Doug Lyman DVM, DACVP

In an earlier article, clinical copper toxicity in Holstein heifers was described. It now appears that copper is accumulating in the livers of all age groups of Wisconsin Holsteins and may be causing, at the very least, subclinical liver damage. A recent review of 225 Wisconsin Veterinary Diagnostic Laboratory (WVDL) submissions, for which ICP-MS liver metals analysis was performed, revealed a mean copper across all age groups (except fetuses, which also showed some elevated levels) of 143 ppm wet weight (ww). Normal equals 25 to 100 ppm ww.

Histologic examination reveals an abundance of rhodanine-stainable copper in liver-tissue samples. Rhodanine stains only copper that is not complexed to metallothionein. The median was 130 ppm ww. Animals from 1 to 20 months actually had higher levels (173 ppm ww) than adults (145 ppm ww). The literature suggests that in species susceptible to copper accumulation and toxicity, including cattle, humans, dogs, sheep and rats, subclinical damage becomes apparent at around 150 ppm ww while the threshold for clinical toxicity occurs, with much individual variation, at levels above 250 ppm ww.

It was considered that, by virtue of prior illness, this may have represented a skewed population, so 30 liver samples were randomly collected at a cull cow slaughter plant. The samples may have included a few beef and colored dairy cows. The mean liver copper of these 30 samples was 163 ppm ww, while the median was 150 ppm ww.


Histologic examination reveals an abundance of rhodanine-stainable copper in liver-tissue samples. Rhodanine stains only copper that is not complexed to metallothionein.

The production and release of the circulating, copper-containing protein ceruloplasmin by the liver is increased during an acute-phase response, perhaps drawing down liver copper during some illnesses and potentially explaining why the WVDL submissions tended to be lower. Histologic examination revealed an abundance of rhodanine-stainable copper (see image) in many of both populations. Rhodanine stains only copper that is not complexed to metallothionein, the normal storage protein, thus suggesting that any stainable copper represents excess and is potentially detrimental. A spectrum of mild histologic lesions representing non-specific insult was present in many livers.

As something of a footnote, the United Kingdom has, over the past 10 years, encountered a serious problem with clinical copper toxicity including significant mortality in Holstein cows. This came about as a result of over supplementation (often in the range of 25-35 ppm of the total diet) due to concerns about molybdenum interference with copper absorption. A large (n = 2250) survey of adult Holsteins revealed a mean liver copper of 130 ppm ww. It was also found that liver damage, as determined by elevated serum levels of the leakage enzyme glutamate dehydrogenase, began at around 150 ppm ww and that these levels dropped as copper was withdrawn from the diet.

Similar histologic lesions were also documented. One of their, albeit unsubstantiated, suggestions was that black and white cows (to include Friesians) may be genetically increasing in susceptibility to copper accumulation. Is this a possible explanation for the high levels we’ve seen in young Holsteins? Perhaps the situation is not unlike that in dogs wherein an increasing number of breeds appear to be prone to copper accumulation though, in some, the question of cause or effect remains to be sorted out. Or is copper being overfed here also? Do chelated or proteinated supplements contribute? Are levels going up in home-raised feeds and forages as a result of all the copper sulfate entering the system on many farms? Could it be a combination of all the above?


TB comes in small packages too

Dr. Cindy Bell Diagnostic Pathologist DVM, University of Wisconsin-Madison 2008 Diplomate ACVP

Dr. Cindy Bell
Diagnostic Pathologist
DVM, University of Wisconsin-Madison 2008
Diplomate ACVP


TB comes in small packages too

By C. Bell, DVM, DACVP

Strange as it is, one species that the pathologists at WVDL autopsy fairly frequently is the Budgerigar….you know, Budgies….“parakeets”…..those fairly inexpensive but attractive small versions of parrots.  Like parrots, they belong to the family of birds called psittacines.  Many older budgerigars we see have cancer, frequently of the reproductive tract.  In fact, ovarian carcinoma occurs in aged females of many species of birds.  I and others happen to think that it is an underexplored animal model for human ovarian cancer.   But I digress….the most memorable budgerigar autopsy that I have performed was not a cancer case.  While performing this particular autopsy, which is a “gross” post-mortem examination, I saw no tumor, no evidence of disease, not a single clue as to why the bird was sick and died.

This happens to pathologists a lot, but we don’t despair.  “That is why God created a microscope,” says an old pathologist friend, meaning that we perform histopathology, a “microscopic” post-mortem examination.  As I was looking at the glass microscope slides of this little bird’s tissues, I saw something that was not readily recognizable as a particular organ.  There were large cells, and these cells were stuffed full of something….something very small and very hard to see.  I had a hunch.  I ordered a special acid fast slide to be made, which made the little rod bacteria within the cells stand out like hot flamingo-pink confetti.  The cells were stuffed with these “acid fast bacilli” bacteria and the tissue was the sorry remains of this bird’s adrenal gland.

Although not strictly accurate, “acid fast bacilli” is synonymous with bacteria of the genus Mycobacterium.  The most famous is Mycobacterium tuberculosis, the case of Tuberculosis in humans.  There are many other species, some more important than others.  Mycobacterium bovis is the cause of Bovine Tuberculosis, a disease for which we monitor and hope not to see in Wisconsin.  Mycobacterium paratuberculosis causes Johnes Disease in ruminants.  There are other Mycobacterium species and subgroups.  Each tends to have a predilection for a certain group of animal ( birds, rodents, aquatic animals, etc.) yet has the potential to infect a broad range of species, including humans.   Immune-suppressed or immune-compromised humans are most at risk.  As a percentage of our modern population, this group of people is large and continues to grow each year.  Included are people with AIDS, transplant recipients, chemotherapy patients, and people treated for a broad array of immune system disorders.  A final key fact about Mycobacterium is that infections are very difficult to detect and may be impossible to cure.

So, there was my budgie with a Mycobacterium infection, an infection that is not particularly rare in birds, reptiles, aquatic animals, and even some mammals.  Nevertheless, I called the veterinarian who had submitted the bird to WVDL for diagnosis.  After contacting the bird’s owner, the submitting veterinarian and I were again on the phone discussing the implications of the bird having come from a household that included 1. Another bird and, 2. A human family member with a chronic disease condition.  Ultimately, the WVDL sent tissue to the National Veterinary Services Laboratory in Ames, IA.  There, they identified the species of Mycobacterium in the bird.  Fortunately, it was not Mycobacterium tuberculosis or another species known to typically infect humans.  However, the other bird in the household was likely to harbor the infection even if it never got sick, leaving the family with a tough decision regarding the future of the remaining pet bird.



Mysterious virus found in Wisconsin trout

State officials worry about impacts, but release infected fish

State natural resource officials are wondering how a mysterious virus found  its way to Wisconsin trout and what it will mean for the health of aquatic  life.

“It’s a big unknown,” said Susan Marcquenski, a fish health specialist for  the state Department of Natural Resources. “There’s very little information  about the effect of the virus on cool-water species.”

Read more:


A Brief Tour of the Chemistry Section of WVDL

A Brief Tour of the Chemistry Section of WVDL


The chemists at WVDL have the use of sophisticated instrumentation.  These types of equipment are considered the norm in a diagnostic chemistry lab and are invaluable workhorses.    Here is a very brief introduction of some of our more important instruments:


HPLC: High Performance Liquid Chromatograph

Liquid chromatography is used to separate non-volatile (not easily vaporized) analytes from one another by using high-pressure pumps to push the analyte liquid through a packed column in a solvent (mobile phase).  The analytes in the sample react differently to the column packing, causing each to spend a different amount of time in the column before being pushed out by the mobile phase (retention time).  The order in which the analytes are detected, and the retention times at which they are detected, help us to identify the various chemical species in the analyte.


Our HPLC is equipped with a UV detector, and is primary used for Vitamin A and Vitamin E analyses of serum and livers.


HPLC/MS: High Performance Liquid Chromatograph-Mass Spectrometer

This instrument is an HPLC fitted with a mass spectrometer detector.  This instrument takes separated chemical species, fragments them, then precisely separates and quantifies them by mass.  LC/MS is the workhorse of non-volatile drug and pesticide analysis.


We use our LC/MS to analyze the following: taurine, anticoagulants (rodenticides), ionophores, and non-volatile pesticides.


HPIC: High Performance Ion Chromatograph

Much like HPLC, the HPIC consists of pumps, a packed column, and a detector.  In this case, the column separates anions (or cations) based on charge via ion-exchange reactions.


We use our HPIC for anion analysis: primarily nitrites, nitrates and sulfates.


GC/MS: Gas Chromatograph-Mass Spectrometer

Gas chromatography works similarly to liquid chromatography, except everything is in the gaseous phase.  The organic sample is volatilized-vaporized and pushed through a long, hollow-core column (about 30 meters) by an inert gas (usually helium).  The order and time at which the analyte species are eluted from the column helps to identify them.  Our GC is fitted with a MS detector, which quantifies the mass of each analyte as it elutes from the column.  We have access to a large electronic library of chemicals (200,000+ compounds) within the software which can match the precisely measured mass spectra to those in the library, thus identifying the analytes.


Our GC/MS is used for detection of chemicals which can be volatilized within the drug and pesticide groups, and also for ethylene glycol analyses.


ICP-MS: Inductively-Coupled Plasma Mass Spectrometer

This instrument ionizes liquid samples (dilute fluids or digested tissues) via very hot Argon plasma (~10,000o Kelvin).  The ions are then separated by mass and counted by the pulse count detector (for trace elements) or the analogue detector (for more concentrated macro elements).  By separating and counting the number of atoms at each mass of interest, we can determine the concentration of each element of interest.


We use our ICP-MS for element-mineral panel analyses, as well as individual metal-mineral analyses if requested.


And there you have it:  a broad overview of what some of these instruments do, and how we use them here in the Chemistry section of WVDL.  These pieces of equipment require considerable care and maintenance, both preventative and day-to-day.  We keep them working their best and optimized in order to provide our clients with accurate results and in order to keep them running for years to come.




Pet food safety is an issue on the minds of all pet owners

Stay on top of all the latest pet food recalls, listed here by the FDA (click the Animal Health tab).

Join their email list to get regular recall updates as well.

Sodium Toxicity in Neonatal Dairy Calves

Dr. Donald Sockett Veterinary Microbiologist DVM, Univ. of Guelph, 1981 PhD, Univ. of Wisconsin, 1991 Diplomate, A.C.V.I.M.

Dr. Donald Sockett
Veterinary Microbiologist
DVM, Univ. of Guelph, 1981
PhD, Univ. of Wisconsin, 1991
Diplomate, A.C.V.I.M.


Sodium Toxicity in Neonatal Dairy Calves: 7.24.2013

Recently, the WVDL has confirmed sodium toxicity (salt poisoning) in 4 different dairy herds. All of the calves were less than 14 days of age and died within 6-24 hours after the onset of clinical signs. Neurological disease (abnormal gait, stiffness, muscle twitching, seizures and convulsions) was reported for some calves but for many calves the only observation made by the herd owner was lethargy and depression prior to death. Submitting veterinarians were suspicious of gram-negative septicemia particularly salmonellosis. Morbidity and mortality rates ranged from 25 – 100%. All four herds were feeding commercial milk replacer diets to their calves.

 Some of the calves had diarrhea caused by Cryptosporidium parvum, rotavirus or coronavirus but many calves did not. A few calves had pneumonia or dehydration. There were no consistent gross or histopathological lesions. Brains were often normal in appearance.

 Hypernatremia is defined as a serum or plasma sodium value of 155 mmol/L or higher. Calves are at risk of developing neurological disease when the serum or plasma values exceed 160 mmol/L.  A brain sodium level of 1,800 ppm or higher (wet matter basis) is considered confirmation of sodium toxicosis. Normal brain sodium values are less than 1,400 ppm. Serum, plasma, ocular fluid, CSF, and cerebral cortex are all appropriate samples to test for sodium toxicosis.


Published reports of salt poisoning in neonatal calves have led to the perception that it is caused by one or more of the following risk factors: Commercial oral electrolyte or milk replacer mixing errors, limited or no access to free choice drinking water or potable water with an excessively high concentration of sodium (≥ 500 ppm). Water that has passed through a water softener can have very high concentrations of sodium and should not be used to mix up commercial milk replacer or used as a source of potable water unless it has been tested and verified to have low levels of sodium (≤ 100 ppm).


While one or more of these risk factors were discovered in 2 of the 4 herds, they could not be confirmed in the other 2 herds despite intensive questioning by the herd veterinarians and testing of the milk replacer solution and potable drinking water.  The only risk factor that was identified in these two herds was heat stress causing mild dehydration and feeding a commercial milk replacer diet. Since neonatal calves do not drink much water during the first week of life, this coupled with mild to moderate dehydration may be sufficient to cause sodium toxicosis in some herds.


Sodium toxicosis should be considered for any dairy calf that dies within 4-24 hours of becoming ill that does not have complications of neonatal calf diarrhea (dehydration and metabolic acidosis) or gross lesions which can explain the cause of death such as abomasal tympany, perforating abomasal ulcers, omphalophlebitis, pneumonia, bacterial septicemia and meningoencephalitis. The likelihood of sodium toxicity increases if the calf has neurological disease as well.


It is very important that veterinarians submit the entire brain or cerebral cortex both fresh (≥ 50 grams) and formalin-fixed (≥ 1 x 2 cm slice) to the WVDL, along with serum or plasma for suspected cases of sodium toxicosis.


If sodium toxicosis is found, the WVDL recommends that a 1-2 ounce sample of milk replacer solution be submitted frozen to the Madison lab. It is a good idea to submit samples from two or more feedings particularly when more than one person is responsible for feeding the calves. Submitters should request analysis for percent total solids, sodium concentration and osmolality. In addition, a sample of potable water should be sent to a private laboratory for testing which includes sodium concentration of the water.

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